In a previous paper1-3, a series of 1-benzyl-3-(5′-hydroxymethyl-2′-furyl)indazole (YC-1) derivatives were found to exhibit significant inhibitory effect against thrombin-, AA-, collagen-, and PAF-induced platelet aggregation. The broad-spectrum anti-platelet activity of YC-1 derivatives indicated that they interfered with platelet aggregation through a common pathway. Mechanism investigation revealed that such anti-platelet activity was associated with NO-independent activation of soluble guanyl cyclase (sGC)1,2. YC-1 was long recognized as a new anti-platelet agent with unique mechanism of action. Since the debut of our YC-1 paper, more than 150 publications related with YC-1 have been seen in the literature. Documented in these papers were the versatile pharmacological activities of YC-1 that include its anti-platelet and vasodilatorly activity via cGMP-dependent mechanisms. On the contrary, YC-1 was also reported to exert its anticancer and anti-angiogenic effects through a cGMP-independent pathway4. Thus, YC-1 has been recognized as an innovative drug candidate with great potential.